Memphis Integral Neurofeedback Institute

Does Neurofeedback really work for ADD/ADHD?

A Guide to the Outcomes Research

Five to ten percent of America’s children struggle with an attentional disorder. Many of them are prescribed psychostimulant medications that help them be still and focus better. Research has consistently shown these medications to be helpful for 60-70% of these children. In fact, the use of psychostimulants has been so successful that 90% of the annual production of methylphenidate is consumed by America’s children.

Unfortunately, for 30-40% psychostimlants have little or no impact on ADD/ADHD symptoms. For the rest there is a risk of side effects such as nausea, loss of appetite, headaches, and even growth problems. And since the positive effects of stimulant drugs on the symptoms of ADHD are state dependent, once the drugs wear off, the symptoms return.

These factors have prompted researchers to look for other, more effective treatments for ADD/ADHD. In the 1970s Dr. Joel Lubar of the University of Tennessee, Knoxville, began using Neu-rofeedback Training (also known as EEG biofeedback) to treat ADD/ADHD. Since then he and other researchers have developed Nurofeedback Training into a very successful treatment option that has proven to have long-term positive results in follow-up studies up to ten years after treatment was completed.

The most recent research shows compelling evidence for a treatment approach that combines the use of psychostimulant medications and parent/teacher training with Neurofeedback Training for long-term positive results. The following is just a small sample of some of the published research available on the use of neurofeedback for ADD/ADHD.

Linden, M., T. Habib, and V. Radojevic “A Controlled Study of the Effects of EEG Biofeedback on Cognition and Behavior of Children with Attention Deficit Disorders and Learning Disabilities.” Biofeedback and Self Regulation 2 (1996): 35-49.

This study involved 18 children between the ages of 5 and 15 split into a treatment group and a control group. None of the children received traditional therapy or psychostimulants during the study. The treat-ment group received 40 bi-weekly neurofeedback sessions in which faster Beta brainwaves (16-20Hz) were reinforced and slower Theta waves (4-8Hz) and muscle tension (EMG) were suppressed.

After treatment was completed the chil-dren who received neurofeedback had a mean increase in their Composite K-BIT IQ scores of 9 points greater than the control group. In addition, hyperactive and aggres-sive-defiant symptoms decreased for those in the treatment group.

Lubar, J. F.
“Psychophysiology and Biofeedback Treatment for Attention Deficit/Hyperactivity Disorder.” AAPB White Paper (1995).

Lubar’s 1995 paper presents some of the basic facts about ADHD and summarizes some of the neurological markers of ADHD including an overabundance of slower brain waves centrally and frontally, and decreased fast activity centrally and posteriorly. Lubar goes on to summarize reports that after neu-rofeedback children tend to be “much more attentive in classroom situations, less impul-sive in the home setting, and less hyperac-tive in home, school, and in playground settings.”

Lubar, J. F. “Neocortical Dynamics: Implications for Under-standing the Role of Neurofeedback and Re-lated Techniques for the Enhancement of Attention.” Applied Physiology and Biofeedback 22 (1997): 111-126.

The research of the ‘decade of the brain’ in the 1990s led to a much greater under-standing of how EEG is generated by the brain. This greater understanding helps explain how neurofeedback works through the EEG to correct brain dysfunction. According to Lubar “the cortex works in terms of resonant loops.” Local resonances produce 30Hz EEG frequencies. Regional resonances produce Alpha and Beta EEG frequencies. Global resonances produce Delta and Theta frequencies. These resonances are either spontaneous or originate from thalamic pacemakers. EEG, then, is gener-ated in the cortex itself and by the thalamus. This means EEG reflects “cortical organiza-tion . . . the dynamics that are occurring at the cortex and thalamus and the relation-ship between these dynamics, different behavioral states, mood states, psychopathology, and learning.” Neurofeedback ameliorates the symptoms of ADHD be-cause it “changes cortical and thalamocorti-cal dynamics.”

Lubar, J. F., M. O. Swartwood, J. N. Swart-wood, and P. H. O’Donnell
“Evaluation of the Effectiveness of EEG Neuro-feedback Training for ADHD in a Clinical Setting as Measured by Changes in T.O.V.A. Scores, Be-havioral Ratings, and WISC-R Performance.” Biofeedback and Self-Regulation 20 (1995): 83-99.

In the introduction to this study Lubar refers to the symptoms of inattention, impulsivity, and hyperactivity as secondary outcomes of the neurological disorder that underpins ADHD. This neuropathy is the target of neurofeedback treatment and the subsequent studies presented in this article provide more evidence for its effectiveness. The three part study looked at neurofeedback’s impact on continuous performance test scores, behavior ratings, and IQ scores. All three studies supported the use of neurofeedback in treating ADHD. Children who demonstrated EEG changes after neurofeedback treatment improved on 3 out of 4 of the continuous performance test scales. Parent reports on the ADDES showed significant behavioral improvements. IQ scores increased by a group mean of 9 points of the WISC-R Full Scale IQ.

Lubar, J. F., M. O. Swartwood, J. N. Swart-wood, and D. L. Timmermann
“Quantitative EEG and Auditory Event-Related Potentials in the Evaluation of Attention-Deficit/Hyperactivity Disorder: Effects of Methylphenidate and Implications for Neurofeedback Training.” Journal of Psychoeducational As-sessment, ADHD Special (1995).

In this special issue of the Journal of Psychoeducational Assessment Dr. Lubar and his colleagues present four studies that support the neurological basis for ADHD. The first study involved 112 subjects between the ages of 8 and 46 and a control group. Each of the subjects was diagnosed with ADHD by independent assessment. Quantitative EEG recordings were made of each subject using 19 electrodes in the standard 10-20 international electrode placement system. The Lexicor Medical Technology Neu-rosearch 24 instrument was used to measure EEG under six conditions. After recording, all muscle movement artifact was removed from the data and Fourier power spectral analysis was used to obtain the percentage power measurements of Theta and Beta ac-tivity. In this way Lubar, et al., were able to demonstrate that Theta/Beta ratios for indi-viduals with ADHD are higher than those for non-ADHD individuals and thereby support the use of Theta/Beta ratios as an effective means of diagnosis for ADHD.

In the second study the researchers again used the same techniques and instruments to measure the quantitative EEG of boys under two conditions: 30 minutes after the administration of methylphenidate and 48 hours after the administration of methyl-phenidate (each child’s dose had been ti-trated by the child’s own physician and was at a level for optimum behavioral impact). Age-matched controls were also used. The QEEG measurements showed that the methylphenidate had no effect on Theta/Beta ratios, the underlying cause of ADHD in 60-70% of cases.

The third study involved 17 males be-tween the ages of 9 and 11 and 18 matched controls. Each of the subjects had been diagnosed with ADHD by a physician, did not have comorbid learning disabilities, were being treated with methylphenidate, and parents rated them in the clinically significant range on at least one subscale of the McCarney Attention Deficit Disorder Evaluation Scale (ADDES). Testing was performed under the use of methylphenidate and 48 hours after the last dose. Event-related potentials (ERPs) were collected in order to assess habituation to repeated stimuli present in individuals with ADHD. Lexicor NRS24 and Lexicor evoked potential software was used. EEG was measured at the central midline locations using the international 10-20 system. This study showed that children with ADHD do indeed become habituated over time to a repeated stimulus in a way that non-ADHD do not. The study also showed that methylphenidate did not impact the performance of the ADHD children.

Finally, the fourth study explored the ef-fect of neurofeedback training on the quan-titative EEG of 17 children diagnosed with ADHD between the ages of 8 and 15. Each subject was trained to decrease Theta and increase Beta with electrodes placed along the midline at FCZ and PCZ. Eleven of the children were ultimately able to successfully decrease Theta and increase Beta. Both percentage and microvolt levels of Theta were decreased while the percentage of Beta was increased, thereby improving the Theta/Beta ratios of the successful subjects.

Ultimately, Lubar and his colleagues concluded that, “Neurofeedback, when in-tegrated with medication, can lead to a much more profound and long lasting effect than either approach in isolation.

Monastra, V. J., D. M. Monastra, and S. George.
“The Effects of Stimulant Therapy, EEG Biofeed-back, and Parenting Style on the Primary Symp-toms of Attention-Deficit/Hyperactivity Disorder.” Applied Psychophysiology and Bio-feedback 27 (December 2002): 231-249.

The preliminary reports of this impor-tant study were presented at the 11th Annual Conference of CH.A.D.D. in October of 1999 and the Annual Convention of the American Psychological Association in August of 2000. The study looked at how neu-rofeedback, methylphenidate, and parenting style worked in conjunction to impact ADHD. To do so the researchers studied 100 children between the ages of 6 and 19 and their parents. The children were divided into two groups. One group, which they called the Comprehensive Clinical Care (CCC) group, received medication management, parent counseling and school con-sultation. The second group was termed the Comprehensive Clinical Care plus EEG Biofeedback (CCC+B) group. This group received everything the CCC group received in addition to receiving EEG neurofeedback using the Autogenics A-620 Neurofeedback System.

Parents and teachers of the children in this study completed the ADDES behavioral rating scale. Pretreatment testing of the children was done at least 48 hours after the administration of any psychostimulant medication. The Test of Variables of Attention (TOVA) was used to measure attention and response time factors. Quantitative EEG data was collected with the Autogenics A-620 instrument and assessment software. All participants in this study tested positive for ADHD on all of the assessment measures.

During the treatment phase of the study all the children were treated with methylphenidate. Parents received 10 parenting classes and additional consultation as needed. Each participant was then evaluated by their school districts and individual educational programs (IEPs) or plans of academic support/accommodation (“504 Plan”) were developed with the consulta-tion of the researchers. Finally, members of the CCC+B group received weekly neurofeedback treatment sessions.

Posttreatment assessments were per-formed one year after the initial intake interview while the children were still taking methylphenidate and again one week after the last dose of the medication. Posttreatment assessments utilized the same tools as the pretreatment: the ADDES, the TOVA, and QEEG measurement.

On the ADDES behavioral measures the CCC group revealed a “pattern of con-tinued impairment both at home and at school.” No sustained improvement was shown after the removal of the methylphenidate. The CCC+B group did show sustained improvement, as reported by both parents and teachers, even when the methylphenidate was no longer in the children’s’ systems.

When retested with the TOVA at posttreatment, both the CCC and the CCC+B group scored in the unimpaired range. However, after the one week period without methylphenidate, the CCC group’s per-formance returned to the pretreatment baseline measure while the group that received neurofeedback, the CCC+B group, continued to score in the unimpaired range.

As expected, pretreatment QEEG measures showed no differences in the amount of cortical slowing between the CCC and CCC+B groups. However, differences did appear in the posttreatment assessments. The CCC+B group showed less cortical slowing than the CCC group even when methylphenidate treatment was stopped.

The researchers in this study concluded that the most effective treatment for ADHD involved a combination of medication, par-ent/school counseling, and neurofeedback training.

Nash, J. K.
“Treatment of Attention Deficit Hyperactivity Disorder with Neurotherapy.” Clinical Electroencephalography 31 (2000): 30-37.

Nash began his review of neurotherapy research with a summary of the rationale for its use including the state dependent effects of psychostimulant medications and their potential side effects, the possibility for the abuse of psychostimulants, the 30-40% of individuals with ADHD for whom psy-chostimulants do not work, and the high rate of comorbid anxiety in as many as 30% of individuals with ADHD. Nash also dis-cussed the lack of evidence of the safety of long-term use of psychostimulants citing the longest follow-up study as 14 months. Thus, the long-term effects of psychostimulants on the brain, the cardiovascular system, and the body’s other systems is currently unknown.

Nash also discusses what he calls the “scientific rationale for neurotherapy.” He reviews the research that demonstrates the neurological basis for ADHD including QEEG, SPECT, and PET studies, all of which corroborate the presence of frontal lobe abnormalities in individuals with ADHD.

Next Nash presents an excellent and succinct description of neurofeedback as it is used to treat ADHD. In neurofeedback the patient’s EEG is operantly conditioned by helping the individual “learn to recognize the small shifts in state they go through during the course of their day.” Nash also describes neurofeedback as “a ‘fine-grained’ form of cognitive behavior modification in which improvements in cortical functions are operationalized as changes in the EEG.” This operant conditioning of the EEG is achieved by monitoring the EEG in real-time and providing computerized feedback in the form of audio and visual signals that reflect the achievement of specific EEG parameters. These signals are often provided in the form of games wherein points are earned when the EEG meets the established parameters.

Finally, Nash provides an excellent review of the outcomes literature on the use of neurofeedback for ADHD. Nash cites the first case study published in 1976 by Lubar and Shouse in which an 11 year-old boy was taught to increase his SMR and decrease Theta. Subsequent positive changes in the boy’s oppositional behavior, level of cooperation, and ability to focus and stay in his seat at school occurred. In the middle of the case study, and without the boy knowing, the training was reversed and SMR de-creased while Theta increased. As expected, the child’s behavioral and attentional improvements also reversed. Finally, training was returned to therapeutic parameters, SMR once again increased and Theta decreased and the improvements returned. After neurofeedback treatment the boy no longer used any medication and continued to function well even years after the completion of neurofeedback treatment and the removal of all medication.

After this first case study, Lubar and Shouse conducted more successful studies using the same ABA reversal design and the same neurofeedback parameters.

In 1983 Michael Tansey published another landmark case study in which neuro-feedback was used to treat a fourth grader with perceptual impairment and hyperactivity. After neurofeedback treatment the boy’s pediatrician was able to stop the use of methylphenidate and the boy was moved out of his special education class into a normal fourth grade class where he raised his grades from 3 As, 3 Bs, and 4 Cs to 4 As, 5 Bs, and 1 C. 10 years after the completion of neurofeedback treatment the boy had finished high school and was in college.

Nash concludes by reviewing many of the research studies from the 1990s, many of which are reviewed here, that show consistently positive and long-term results of neurofeedback on ADHD.

Ramirez, P. M., D. Desantis, and L. A. Opler
“EEG Biofeedback Treatment of ADD: A Viable Alternative to Traditional Medical Intervention?” Annals of the New York Academy of Sciences 931 (June 2001): 342-358.

This literature review looked at the published research on the use of neurofeedback for ADHD. The authors used Psychlit and Medline searches to obtain articles that dated as far back as 1968. After their thorough review, the authors concluded that while Alpha training does not appear to be effective for treating ADHD, SMR training and Theta/Beta training (the two training paradigms reviewed here) do seem to be ef-fective in ameliorating the behavioral and cognitive symptoms of ADHD.

Rossiter, T. R., and T. J. LaVaque
“A Comparison of EEG Biofeedback and Psy-chostimulants in Treating Attention Defi-cit/Hyperactivity Disorders.” Journal of Neurotherapy (1995): 48-59.

This study involved two treatment groups of 23 patients each. One group was made up of individuals with ADHD who were treated with psychostimulant medica-tions. Individuals in the medication group were treated with either methylphenidate or dextroamphetamine as determined by their physicians.

The second group consisted of individuals with ADHD who received neurofeedback as their treatment using the Lexicor Medical Technology instruments in 3-5 sessions per week. Individuals were told to increase Beta or SMR while inhibiting Theta. Both groups also received other supportive treatments such as parent training.

Posttreatment testing revealed that both groups improved their TOVA scores. Furthermore, the neurofeedback group experienced improvement of cognitive and behavioral symptoms of ADHD that generalized to home and school settings.

Sterman, M. B. “EEG Markers for Attention Deficit Disorder: Pharmacological and Neurofeedback Applica-tions.” Child Study Journal 30 (2001): 1-23.

Sterman used numerous studies (including many of his own as well as those performed by others) to summarize the neurological patterns shown to be associated with ADHD. He looked at QEEG studies as well as brain imaging and genetic studies to identify “three basic and some-times overlapping patterns of QEEG abnormality in children diagnosed behaviorally as having ADD.” The first pattern associated with ADHD is that of dominant and generalized slowing of the EEG regardless of attentional state. The second pattern is “highly coherent, slow activity shown in frontal and particularly pre-frontal areas.” This frontal slowing increases upon task engagement (a non-ADHD brain would decrease frontal slowing when engaged in a task). Finally, a third pattern involves increased central and parietal Alpha.

From this summary of EEG markers for ADHD, Sterman draws conclusions regarding treatment. Because individuals exhibiting each pattern respond better to different psychostimulants, EEG measurements can provide greater precision in the use of such medications. Neurofeedback can be used to normalize the above EEG dysfunctions and result in reduced or even eliminated ADHD symptomology.

Swartwood, M. O., J. N. Swartwood, J. F. Lubar, D. L. Timmermann, A. W. Zimmer-man, and R. A. Muenchen
“Methylphenidate Effects on EEG, Behavior, and Performance in Boys with ADHD.” Pediatric Neu-rology 18 (1998): 246-250.

This study used the ADDES, EEG measures, and TOVA to evaluate the effectiveness of methylphenidate on a group of 23 boys aged 9-11. ADDES ratings showed the boys exhibited improved behavior with the use of methylphenidate. The boys also improved their TOVA scores with the use of the medication. However, no global changes in the EEG were seen when medi-cation was used.